Abstract
Aim. The purpose of current research was to assess changes in endothelial progenitor cells (EPC) counts and angiogenic factors levels during atorvastatin therapy in different doses in patients with ischemic heart disease (IHD) as an independent predictor of cardiovascular morbidity and mortality. Methods and Results. The main group included 58 patients with IHD during atorvastatin therapy. EPC quantity (CD34+/CD133+/CD309+ phenotype) was measured by flow cytometry two times – before treatment and 3 months after. Vascular endothelial growth factor (VEGF), C-reactive protein (CRP), monocyte chemoattractant protein-1 (MCP-1), endostatin levels and lipid profile were also measured twice. The control group consisted of 15 healthy volunteers with the same analyzes performed once. Atorvastatin therapy in IHD patients within three months of treatment caused a significant (72% on average) increase of EPC counts (p<0.05). Dependence of EPC gain on statin dose was not reliable (p=0.10), but it was higher when initial EPC counts were low (p=0.01). The therapy showed reliable reduction of VEGF level (by 11%, p<0.01), CRP – by 26% (p<0.01), total cholesterol (TCh) – by 30% (p<0.01), low density lipoprotein (LDL-C) – by 35% (p<0.01), triglycerides (TG) – by 18% (p<0.01), while endostatin, MCP-1 and high density lipoprotein (HDL-C) levels did not change. Correlations between the EPC, TCh and LDL-C changes during therapy were revealed: higher EPC counts gain was associated with higher TCh (p=-0.37, r<0.01) and LDL-C (p=-0.41, r<0.01) levels decrease. Conclusion. We found a significant increase of EPC counts in IHD patients when treated with atorvastatin for 3 months, without statistically reliable difference depending on dosage.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.